Impaired cell proliferation with increased inflammatory response is a hallmark feature of cell senescence associated with COPD pathogenesis.[27] The lung tissues of PPE‐treated PRMT1+/− mice exhibited upregulated expression of senescence‐related genes, including p16, p21, Tnf‐α, Ccl‐2, and Il‐6, as well as increased activity of senescence‐associated β‐galactosidase (SA‐β‐Gal; Figure 7B–D). This evidence concerns the gene CCL2 and chronic obstructive pulmonary disease.